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Articles by A. Mari
Total Records ( 2 ) for A. Mari
  A. Mari , A. Tura , G. Pacini , A. Kautzky-Willer and E. Ferrannini
 

Aims Acute insulin release (AIR) in response to intravenous glucose injection (IVGTT) can be abolished in diabetic subjects when their response to oral glucose is maintained. To elucidate this phenomenon, we examined the relationships between fasting plasma glucose (FPG) and the secretory responses to an IVGTT and an oral glucose test (OGTT).

Methods We measured AIR and secretion after a 75-g OGTT in 221 subjects [age 37±11years, body mass index (BMI) 28±5kg/m2; mean± SD] with normal glucose tolerance (NGT, n=147), impaired FPG/impaired glucose tolerance (IFG/IGT, n=28) and Type 2 diabetes (n=46). Insulin secretion was calculated by C-peptide deconvolution; pancreatic B-cell glucose sensitivity was obtained by OGTT modelling.

Results Both AIR [186 (185), 142 (164) and 10 (16)pmol/l, median (interquartile range)] and B-cell glucose sensitivity [98 (64), 66 (53) and 16 (20)pmol min−1 m−2 l mmol−1] decreased across glucose tolerance category (P<0.0001). However, AIR became ~0 at ~7mmol/l FPG, whereas B-cell glucose sensitivity declined gradually throughout the FPG range. In addition, for FPG >7mmol/l, AIR was no longer related to FPG, whereas a strong relationship between FPG and B-cell glucose sensitivity was preserved (?=−0.71, P<0.0001). In a multivariate regression model, adjusting for sex, age and BMI, glucose sensitivity [standardized regression coefficient (std.r.)=−0.67, P<0.0001], but not AIR (std.r.=0.03, P=0.55), was an independent predictor of FPG.

Conclusions AIR vanishes at fasting or 2-h glucose levels, at which levels some B-cell glucose sensitivity is retained; therefore, AIR has a limited ability to quantify B-cell function in hyperglycaemic states.

  K. G. Brodovicz , J. M. Dekker , J.M. Rijkelijkhuizen , T. Rhodes , A. Mari , M. Alssema , G. Nijpels , D.E. Williams-Herman and C. J. Girman
  Aims  The Finnish Diabetes Risk Score (FINDRISC) is widely used for risk stratification in Type 2 diabetes prevention programmes. Estimates of β-cell function vary widely in people without diabetes and reduced insulin secretion has been described in people at risk for diabetes. The aim of this analysis was to evaluate FINDRISC as a tool to characterize reduced β-cell function in individuals without known diabetes. Methods  In this population-based cohort from the Hoorn municipal registry, subjects received an oral glucose tolerance test and a meal tolerance test on separate days, in random order, within 2 weeks. One hundred and eighty-six subjects, age 41-66 years, with no known Type 2 diabetes were included. Of those, 163 (87.6%) had normal glucose metabolism and 23 (12.4%) had abnormal glucose metabolism (19 with impaired glucose metabolism; four with newly diagnosed Type 2 diabetes based on study results). Insulin sensitivity and β-cell function (classical: insulinogenic index; ratio of areas under insulin/glucose curves; model-based: glucose sensitivity; rate sensitivity; potentiation) estimates were calculated from oral glucose tolerance test and meal tolerance test data. Results  FINDRISC was associated with insulin sensitivity (r = -0.41, P < 0.0001), insulin/glucose areas under the curve (meal tolerance test: r = 0.29, P < 0.0001; oral glucose tolerance test: r = 0.21, P = 0.01) and potentiation factor (meal tolerance test: r = 0.21, P = 0.01). After adjusting for insulin sensitivity, these associations with β-cell function were no longer significant. Conclusions  After adjustment for insulin sensitivity, FINDRISC was not associated with reduced β-cell function in subjects without known Type 2 diabetes. While insulin secretion and insulin sensitivity are both components in Type 2 diabetes development, insulin sensitivity appears to be the dominant component behind the association between FINDRISC and diabetes risk.
 
 
 
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